Stimulation of renin by acute selective chloride depletion in the rat

H. E. Abboud, R. G. Luke, J. H. Galla, T. A. Kotchen

Research output: Contribution to journalArticle

23 Citations (Scopus)

Abstract

/:: (/) √ To determine whether acute chloride depletion per se stimulates renin, we produced selective chloride depletion without sodium depletion in rats by peritoneal dialysis (PD) against 0.15 m NaHCO3 or 0.15 M NaNO3. Control rats were dialyzed against 0.15 M NaCl. Plasma renin activity (PRA) was measured before (PRA1) and 105 minutes after (PRA2) PD. Plasma volume was expanded after PD by infusion of salt-free albumin and was measured immediately after PRA2 by [131]albumin. In experiment 1, rats were prepared on a normal diet. PRA2 (7.0±1.0 ng/ml per hr, mean±SEM) was increased (P<0.05) over PRA1 (4.7±0.7 ng/ml per hr) in Cl-depleted but not in control rats (PRA1=5.3±0.7, PRA2=6.1±0.7, P=NS). In experiment 2, to produce greater chloride depletion, all rats were prepared for 2 wk on a low salt diet. PRA2 (47±5 ng/ml per hr) was increased as compared to PRA1 (24±2 ng/ml per hr, P<0.005) in the Cl-depleted group but not in the control group (PRA1=24±3, PRA2=27±6 ng/ml per hr, P=NS). Serum potassium and final plasma volume were slightly but not significantly lower than controls in these Cl-depleted rats. To exclude an additive effect of these two stimuli for renin, in experiment 2 a we infused chloride-depleted rats with three times as much albumin as controls and with KHCO3, 100 mEq/liter. Despite volume expansion and potassium loading, PRA2 (41±6 ng/ml per hr) was significantly elevated as compared to PRA1 (25±4 ng/ml per hr, P<0.01). Since acute metabolic alkalosis also was present in all Cl-depleted renin-stimulated rats, an additional group (2b) was dialyzed against 0.15 M NaNO3; final plasma arterial pH (7.43) was not different from controls (7.42). Nevertheless, PRA2 levels again were higher (36±6 ng/ml per hr, P>0.05) as compared to PRA1 (23±4 ng/ml per hr). In all experiments, arterial blood pressure, glomerular filtration rate, and filtered sodium load were not different. Free water reabsorption was lower in Cl-depleted than in control rats. We conclude that acute selective chloride depletion per se is a potent stimulus for renin release.

Original languageEnglish (US)
Pages (from-to)815-821
Number of pages7
JournalCirculation Research
Volume44
Issue number6
StatePublished - 1979
Externally publishedYes

Fingerprint

Renin
Chlorides
Peritoneal Dialysis
Albumins
Sodium
Parenteral Infusions
Plasma Volume
Glomerular Filtration Rate
Arterial Pressure
Salts
Diet
Water

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Abboud, H. E., Luke, R. G., Galla, J. H., & Kotchen, T. A. (1979). Stimulation of renin by acute selective chloride depletion in the rat. Circulation Research, 44(6), 815-821.

Stimulation of renin by acute selective chloride depletion in the rat. / Abboud, H. E.; Luke, R. G.; Galla, J. H.; Kotchen, T. A.

In: Circulation Research, Vol. 44, No. 6, 1979, p. 815-821.

Research output: Contribution to journalArticle

Abboud, HE, Luke, RG, Galla, JH & Kotchen, TA 1979, 'Stimulation of renin by acute selective chloride depletion in the rat', Circulation Research, vol. 44, no. 6, pp. 815-821.
Abboud HE, Luke RG, Galla JH, Kotchen TA. Stimulation of renin by acute selective chloride depletion in the rat. Circulation Research. 1979;44(6):815-821.
Abboud, H. E. ; Luke, R. G. ; Galla, J. H. ; Kotchen, T. A. / Stimulation of renin by acute selective chloride depletion in the rat. In: Circulation Research. 1979 ; Vol. 44, No. 6. pp. 815-821.
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N2 - /:: (/) √ To determine whether acute chloride depletion per se stimulates renin, we produced selective chloride depletion without sodium depletion in rats by peritoneal dialysis (PD) against 0.15 m NaHCO3 or 0.15 M NaNO3. Control rats were dialyzed against 0.15 M NaCl. Plasma renin activity (PRA) was measured before (PRA1) and 105 minutes after (PRA2) PD. Plasma volume was expanded after PD by infusion of salt-free albumin and was measured immediately after PRA2 by [131]albumin. In experiment 1, rats were prepared on a normal diet. PRA2 (7.0±1.0 ng/ml per hr, mean±SEM) was increased (P<0.05) over PRA1 (4.7±0.7 ng/ml per hr) in Cl-depleted but not in control rats (PRA1=5.3±0.7, PRA2=6.1±0.7, P=NS). In experiment 2, to produce greater chloride depletion, all rats were prepared for 2 wk on a low salt diet. PRA2 (47±5 ng/ml per hr) was increased as compared to PRA1 (24±2 ng/ml per hr, P<0.005) in the Cl-depleted group but not in the control group (PRA1=24±3, PRA2=27±6 ng/ml per hr, P=NS). Serum potassium and final plasma volume were slightly but not significantly lower than controls in these Cl-depleted rats. To exclude an additive effect of these two stimuli for renin, in experiment 2 a we infused chloride-depleted rats with three times as much albumin as controls and with KHCO3, 100 mEq/liter. Despite volume expansion and potassium loading, PRA2 (41±6 ng/ml per hr) was significantly elevated as compared to PRA1 (25±4 ng/ml per hr, P<0.01). Since acute metabolic alkalosis also was present in all Cl-depleted renin-stimulated rats, an additional group (2b) was dialyzed against 0.15 M NaNO3; final plasma arterial pH (7.43) was not different from controls (7.42). Nevertheless, PRA2 levels again were higher (36±6 ng/ml per hr, P>0.05) as compared to PRA1 (23±4 ng/ml per hr). In all experiments, arterial blood pressure, glomerular filtration rate, and filtered sodium load were not different. Free water reabsorption was lower in Cl-depleted than in control rats. We conclude that acute selective chloride depletion per se is a potent stimulus for renin release.

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